Anorexia is a loss of appetite or a lack of desire for food. Nausea, abdominal pain, and diarrhea may accompany it. Anorexia can result from dysfunction in the GI system or other systems, such as cancer, heart disease, renal disease, or central nervous system dysfunction.

Normally, a physiologic stimulus is responsible for the sensation of hunger. A falling blood glucose level stimulates the hunger center in the hypothalamus; rising blood fat and amino acid levels promote satiety. Hunger is also stimulated by contraction of an empty stomach and suppressed when the GI tract becomes distended, possibly as a result of stimulation of the vagus nerve. Sight, touch, and smell play subtle roles in controlling the appetite center.

In anorexia, the physiologic stimuli are present but the person has no appetite or desire to eat. Slow gastric emptying or gastric stasis can cause anorexia. High levels of neurotransmitters, such as serotonin (may contribute to satiety), and cortisol (may suppress hypothalamic control of hunger) also have been implicated as a cause of anorexia.

Constipation is characterized by hard stools, difficult or infrequent defecation, and a decrease in the number of stools per week. It’s defined
individually because normal bowel habits range from two to three episodes of stool passage per day to one per week. Causes of constipation include dehydration, consumption of a low-bulk diet, a sedentary lifestyle, lack of regular exercise, and frequent repression of the urge to defecate. It’s also an adverse effect of many medications.

When a person is dehydrated or delays defecation, more fluid is absorbed from the intestine, the stool becomes harder, and constipation ensues. High-fiber diets cause water to be drawn into the stool by osmosis, thereby keeping stool soft and encouraging movement through the intestine. High-fiber diets also cause intestinal dilation, which stimulates peristalsis. Conversely, a low-fiber diet contributes to constipation.

Elderly patients typically experience a decrease in intestinal motility and a slowing and dulling of neural impulses in the GI tract. Many older persons restrict fluid intake to prevent waking at night to use the bathroom or because they fear incontinence. This places them at risk for dehydration and constipation.

A sedentary lifestyle, lack of exercise, limitations in physical activity, or inability to engage in physical activity can cause constipation because exercise stimulates the GI tract and promotes defecation. Antacids, opiates, and other drugs that inhibit bowel motility also lead to constipation.

Stress stimulates the sympathetic nervous system, and GI motility slows it. Absence or degeneration in the neural pathways of the large intestine also contributes to constipation. Other conditions, such as spinal cord trauma, multiple sclerosis, intestinal neoplasms, and hypothyroidism, can also cause constipation.

Diarrhea is an increase in the fluidity or volume of feces and the frequency of defecation. Factors that affect stool volume and consistency include water content of the colon and the presence of unabsorbed food, unabsorbable material, and intestinal secretions. Largevolume diarrhea is usually the result of an excessive amount of water, secretions, or both in the intestines. Small-volume diarrhea is usually caused by excessive intestinal motility. Diarrhea may also be caused by a parasympathetic stimulation of the intestine initiated by psychological factors, such as fear or stress.

The three major types of diarrhea are osmotic, secretory, and motility:

♦ osmotic diarrhea—The presence of a nonabsorbable substance such as synthetic sugar or increased numbers of osmotic particles in the intestine increases osmotic pressure and draws excess water into the intestine, thereby increasing the weight and volume of the stool.

♦ secretory diarrhea—A pathogen—such as a bacterial toxin (cholera, Clostridium difficile) or enteropathogenic virus—drugs, or presence of a tumor irritates the muscle and mucosal layers of the intestine. The consequent increase in motility and secretions (water, electrolytes, and mucus) results in diarrhea.

♦ motility diarrhea—Inflammation, neuropathy, or obstruction causes a refiex increase in intestinal motility that may expel the irritant or clear the obstruction.

Dysphagia—difficulty swallowing—can be caused by a mechanical obstruction of the esophagus or by impaired esophageal motility secondary to another disorder. Mechanical obstruction is characterized as intrinsic or extrinsic.

Intrinsic obstructions originate in the esophagus itself. Causes of intrinsic obstructions include tumors, strictures, and diverticular herniations. Extrinsic obstructions originate outside of the esophagus and narrow the lumen by exerting pressure on the esophageal wall. Most extrinsic obstructions result from a tumor.

Distention and spasm at the site of the obstruction during swallowing may cause pain. Upper esophageal obstruction causes pain 2 to 4 seconds after swallowing; lower esophageal obstructions, 10 to 15 seconds after swallowing. If a tumor is present, dysphagia begins with difficulty swallowing solids and eventually progresses to difficulty swallowing semisolids and liquids. Impaired motor function makes both liquids and solids difficult to swallow.

Neural or muscular disorders can also interfere with voluntary swallowing or peristalsis. This is known as functional dysphagia. Causes of functional dysphagia include dermatomyositis, stroke, Parkinson’s disease, or achalasia. (See What happens during swallowing.)

Malfunction of the upper esophageal striated muscles interferes with the voluntary phase of swallowing.

In achalasia, there’s a complete lack of peristalsis within the body of the esophagus. Also, the lower esophageal sphincter doesn’t relax to allow food to enter the stomach. Eventually, accumulated food raises the hydrostatic pressure and forces the sphincter open, and small amounts of food slowly move into the stomach.

Jaundice—yellow pigmentation of the skin and sclera—is caused by an excess accumulation of bilirubin in the blood. Bilirubin, a product of red blood cell (RBC) breakdown, accumulates when production exceeds metabolism and excretion. This imbalance can result from excessive release of bilirubin precursors into the bloodstream or from impairment of its hepatic uptake, metabolism, or excretion. (See Jaundice: Impaired bilirubin metabolism, page 322.) Jaundice occurs when bilirubin levels exceed 2.0 to 2.5 mg/dl, which is about twice the upper limit of the normal range. Lower levels of bilirubin may cause detectable jaundice in patients with fair skin, and jaundice may be difficult to detect in patients with dark skin.

Jaundice in dark-skinned persons may appear as yellow staining in the sclera, hard palate, and palmar or plantar surfaces.

The three main types of jaundice are hemolytic, hepatocellular, and obstructive:

♦ hemolytic (or prehepatic) jaundice—When RBC lysis exceeds the liver’s capacity to conjugate bilirubin (binding bilirubin to a polar group makes it water soluble and able to be excreted by the kidneys), hemolytic jaundice occurs. Causes include transfusion reactions, sickle cell anemia, thalassemia, and autoimmune disease.

♦ hepatocellular (or hepatic) jaundice—Hepatocyte dysfunction limits uptake and conjugation of bilirubin. Liver dysfunction can occur in hepatitis, cancer, cirrhosis, or congenital disorders, and also can be caused by some drugs.

♦ obstructive (or posthepatic) jaundice—When the flow of bile out of the liver (through the hepatic duct) or through the common bile duct is blocked, the liver can conjugate bilirubin, but the bilirubin can’t reach the small intestine.
Blockage of the hepatic duct by calculi or a tumor is considered an intrahepatic cause of obstructive jaundice. A blocked common bile duct is an extrahepatic cause that may be attributed to gallstones or a tumor.

Nausea is feeling the urge to vomit. It may occur independently of vomiting, or it may precede or accompany it. Specific neural pathways haven’t been identified, but increased salivation, diminished functional activities of the stomach, and altered small intestinal motility have been associated with nausea. Nausea may also be stimulated by high brain centers.

Vomiting is the forceful oral expulsion of gastric contents. The gastric musculature provides the ejection force. The gastric fundus and gastroesophageal sphincter relax, and forceful contractions of the diaphragm and abdominal wall muscles increase intra-abdominal pressure. This, combined with the annular contraction of the gastric pylorus, forces gastric contents into the esophagus. Increased intrathoracic pressure then moves the gastric content from the esophagus to the mouth.

Vomiting is controlled by two centers in the medulla: the vomiting center and the chemoreceptor trigger zone (CTZ). The vomiting center initiates the actual act of vomiting. It’s stimulated by the GI tract, from higher brain stem and cortical centers, and from the CTZ. The CTZ can’t induce vomiting by itself. Various stimuli or drugs activate the zone, such as apomorphine, levodopa, digoxin, bacterial toxins, radiation, and metabolic abnormalities. The activated zone sends impulses to the medullary vomiting center, and the following sequence begins:

♦ The abdominal muscles and diaphragm contract.

♦ Reverse peristalsis begins, causing intestinal material to flow back into the stomach, distending it.

♦ The stomach pushes the diaphragm into the thoracic cavity, raising the intrathoracic pressure.

♦ The pressure forces the upper esophageal sphincter open, the glottis closes, and the soft palate blocks the nasopharynx.

♦ The pressure also forces the material up through the sphincter and out through the mouth.

Nausea and vomiting are manifestations of other disorders, such as acute abdominal emergencies, infections of the intestinal tract, central nervous system disorders, myocardial infarction, heart failure, metabolic and endocrinologic disorders, or as the adverse effect of many drugs. Nausea and vomiting can also be present in pregnancy. Vomiting may also be psychogenic, resulting from emotional or psychological disturbance.

The most common disease requiring emergency surgery, appendicitis is inflammation and obstruction of the vermiform appendix (a blind pouch attached to the cecum). Appendicitis may occur at any age, with peak incidence occurring from the late teens to the early 20s. It’s more prevalent in men. Since the advent of antibiotics, the incidence and mortality rate from appendicitis have declined; if untreated, this disease is invariably fatal.

Cholecystitis—acute or chronic inflammation causing painful distention of the gallbladder—is
usually associated with a gallstone impacted in the cystic duct.

Cholecystitis accounts for 10% to 25% of all patients requiring gallbladder surgery. The acute form is most common among middle-aged women; the chronic form, among elderly people. The prognosis is good with treatment.

Cirrhosis is a chronic disease characterized by diffuse destruction and fibrotic regeneration of hepatic cells. As necrotic tissue yields to fibrosis, this disease damages liver tissue and normal vasculature, impairs blood and lymph flow, and ultimately causes hepatic insufficiency. It’s twice as common in men as in women, and it’s especially prevalent among malnourished persons older than age 50 with chronic alcoholism. Mortality is high; many patients die within 5 years of onset.

Crohn’s disease, also known as regional enteritis or granulomatous colitis, is inflammation of any part of the GI tract (usually the proximal portion of the colon and less commonly the terminal ileum), extending through all layers of the intestinal wall. It may also involve regional lymph nodes and the mesentery. Crohn’s disease is most prevalent in adults between ages 20 and 40.

In diverticular disease, bulging pouches (diverticula) in the GI wall push the mucosal lining through the surrounding muscle. Although the most common site for diverticula is in the sigmoid colon, they may develop anywhere, from the proximal end of the pharynx to the anus. Other typical sites include the duodenum, near the pancreatic border or the ampulla of Vater, and the jejunum.

Diverticular disease is common in Western countries, suggesting that a low-fiber diet reduces stool bulk and leads to excessive colonic motility. The consequent increased intraluminal pressure causes herniation of the mucosa.

Diverticular disease of the stomach is rare and is usually a precursor of peptic or neoplastic disease. Diverticular disease of the ileum (Meckel’s diverticulum) is the most common congenital anomaly of the GI tract.

Diverticular disease has two clinical forms:

♦ diverticulosis, in which diverticula are present but don’t cause symptoms

♦ diverticulitis, in which diverticula are inflamed and may cause potentially fatal obstruction, infection, or hemorrhage.

Diverticular disease is most prevalent in men older than age 40 and persons who eat a low-fiber diet. More than one-half of all patients older than age 50 have colonic diverticula.

Popularly known as heartburn, gastroesophageal reflux disease (GERD) refers to backflow of gastric or duodenal contents or both into the esophagus and past the lower esophageal sphincter (LES), without associated belching or vomiting. The reflux of gastric contents causes acute epigastric pain, usually after a meal. The pain may radiate to the chest or arms. It commonly occurs in pregnant or obese persons. Lying down after a meal also contributes to reflux.